Actions of steroid hormones and growth factors on glial cells of the central and peripheral nervous system

Jung-Testas, Ingrid; Schumacher, Michaël; Röbel, P; Baulieu, E E

doi:10.1016/0960-0760(94)90261-5

Cited by 91 publications

(51 citation statements)

References 20 publications

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“…Insulin and IGF-1 levels are decreased in experimental streptozotocin diabetes (23,24) and both are recognized as important stimulating factors for Schwann cells (25)(26)(27).…”

Section: Animalmentioning

confidence: 99%

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Bondan

Lallo

Trigueiro

et al. 2006

Braz J Med Biol Res

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Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 µL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semiquantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 ± 0.77 for oligodendrocytes and 0.67 ± 0.5 for Schwann cells) compared to non-diabetic rats (3.27 ± 0.85 and 1.38 ± 0.81, respectively).

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“…Insulin and IGF-1 levels are decreased in experimental streptozotocin diabetes (23,24) and both are recognized as important stimulating factors for Schwann cells (25)(26)(27).…”

Section: Animalmentioning

confidence: 99%

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Bondan

Lallo

Trigueiro

et al. 2006

Braz J Med Biol Res

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“…As occurs in other estrogen-responsive tissues, in the estrogen-sensitive cells of the normal brain and brain tumors, the binding of estradiol to membrane-associated and intracellular estrogen receptors allows these nonneuronal cells of the central nervous system to respond to estrogens (15)(16)(17)(18); thus, glioma cells are able to respond significantly to estradiol in the culture (33). In addition, previous studies have also shown that the human brain, human neuronal cell lines and glioma cell lines express aromatase and sulfatase and are, therefore, capable of producing estrogens from androgens or estrogen sulfates (19,20,38).…”

Section: Discussionmentioning

confidence: 99%

“…Glioblastoma is the most frequent primary malignant CNS tumor in adults. These tumors express estrogen receptors and also express some of the enzymes involved in the local synthesis of estrogens (17)(18)(19)(20). Expression of aromatase in the brain is involved in the regulatory effects of androgens, via its conversion to estrogens, on neural differentiation, maturation, neural plasticity, neuroendocrine functions and sexual behaviour (21).…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of melatonin on sulfatase and 17β-hydroxysteroid dehydrogenase activity and expression in glioma cells

González

Martínez‐Campa²,

Mediavilla³

et al. 2010

Oncol Rep

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Abstract. Melatonin interacts with estradiol at the estrogen receptor level in different kinds of neoplasias and also regulates the expression and the activity of some enzymes involved in the biosynthesis of estrogens in peripheral tissues. Glioma cells express estrogen receptors and have the ability to synthesize estrogens locally. Since melatonin inhibits the growth of C6 cells, and this indoleamine has been demonstrated to be capable of decreasing aromatase expression and activity in these cells, the aim of the present study was to analyze whether the regulation of the sulfatase, the enzyme that catalyzes the rate-limiting step in the conversion of estrogen sulfates to estrogens, and 17ß-hydroxysteroid dehydrogenase, the enzyme which converts the relatively inactive estrone to the most potent 17ß-estradiol, could be involved in the inhibition of glioma cell growth by melatonin. We found that melatonin decreases the growth of C6 glioma cells and reduces the sulfatase and 17ß-hydroxysteroid dehydrogenase activity. Finally, we demonstrated that melatonin downregulates sulfatase and 17ß-hydroxysteroid dehydrogenase mRNA steady state levels in these glioma cells. By analogy to the implications of these enzymes in other forms of estrogen-sensitive tumors, it is conceivable that their modulation by melatonin may play a role in the growth of glioblastomas.

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“…Insulin and insulin-growth factor (IGF-1) are known to be important stimulating factors for Schwann cells [12][13][14] , but their levels are decreased in experimental streptozotocin diabetes [15][16] . Besides as Schwann cells do not need insulin for glucose transport across membrane hyperglycemia frequently causes intracellular glucose accumulation and increased polyol pathway activity by aldose reductase resulting in increased levels of sorbitol and fructose, which may cause osmotic swelling and cell death 9 .…”

Section: Discussionmentioning

confidence: 99%

Ethidium bromide-induced demyelination in the sciatic nerve of diabetic rats

Bondan

Custódio

Lallo

et al. 2009

Arq. Neuro-Psiquiatr.

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-This study aims to observe the process of myelin loss and repair following the injection of the gliotoxic agent ethidium bromide (EB) in the sciatic nerve of rats previously induced to diabetes mellitus by streptozotocin. Injection of EB was also done in non-diabetic rats. The animals were euthanatized from 3 to 31 days after intraneural injection and nerve sections were collected for ultrastructural study. In nondiabetic rats, Schwann cells (CS) showed signs of intoxication 3 days after, with cytoplasmic vacuolization and rejection of their myelin sheaths. Myelin debris were removed by macrophages in the endoneurium and mast cells were abundant in the lesions. From 14 days following EB injection, supernumerary CS were seen in the expanded endoneurium as well as thin myelin sheaths indicating remyelination. Diabetic rats presented a more extensive myelin vesiculation and segmentar demyelination, with delayed activities from both macrophages and remyelinating SC. No mast cells were noted.KEY WORDS: demyelination, diabetes mellitus, ethidium bromide, peripheral nervous system, remyelination, Schwann cells.desmielinização induzida pelo brometo de etídio no nervo ciático de ratos diabéticos resumo -O estudo visa à observação do processo de perda e reparo mielínico pós-injeção do gliotóxico brometo de etídio (BE) no nervo ciático de ratos previamente induzidos a diabetes mellitus pela estreptozotocina. Injeção de BE foi igualmente realizada em ratos não-diabéticos. Os animais foram eutanasiados dos 3 aos 31 dias pós-injeção intraneural, com colheita de amostras neurais para estudo ultraestrutural. Nos animais não-diabéticos, as células de Schwann (CS) mostraram sinais de intoxicação a partir dos 3 dias pós-gliotóxico, com vacuolização citoplasmática e rejeição de suas bainhas de mielina. Restos mielínicos eram removidos por macrófagos no interior do endoneuro e mastócitos eram abundantes nas lesões. A partir dos 14 dias, CS supranumerárias foram encontradas no endoneuro expandido, além de finas bainhas de mielina indicativas de remielinização. Os ratos diabéticos apresentaram vesiculação mielínica e desmielinização segmentar mais extensas, bem como ausência de mastócitos e atraso na atividade macrofágica e na função remielinizante das CS. PALAVRAS-CHAVE: brometo de estídio, células de Schwann, desmielinização, diabetes mellitus, remielinização, sistema nervoso periférico.

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Actions of steroid hormones and growth factors on glial cells of the central and peripheral nervous system

Cited by 91 publications

References 20 publications

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Delayed Schwann cell and oligodendrocyte remyelination after ethidium bromide injection in the brainstem of Wistar rats submitted to streptozotocin diabetogenic treatment

Inhibitory effects of melatonin on sulfatase and 17β-hydroxysteroid dehydrogenase activity and expression in glioma cells

Ethidium bromide-induced demyelination in the sciatic nerve of diabetic rats

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